Cancer is the general name for a group of more than 100 diseases, which are diagnosed in more than one million new patients in the United States each year. Although there are many kinds of cancer, they share a common feature: abnormal cancer cells either do not undergo efficient apoptosis, and/or are not effectively killed by the patient's immune system, leading to the uncontrolled growth of the abnormal cancer cells. Untreated cancers can cause serious illness and death. Although identification of risk factors, early detection, diagnosis, and treatment options have improved prognosis of many kinds of cancers, cancer remains a leading cause of death.
The p53 tumor suppressor protein plays a critical role in generating cellular responses to a number of stress signals, including DNA damage, aberrant proliferative signals due to oncogene activation, and hypoxia. Upon activation, p53 is stabilized and moves to the nucleus, where it binds to DNA in a sequence specific manner and promotes transcriptional regulation of genes involved in DNA repair, cell-cycle arrest, senescence, and apoptosis. While it is estimated that the p53 gene is mutated in 50% of tumors, increasing evidence reveals that a large percentage of tumors retain wild type p53, but possess other alterations in the p53 pathway, which prevents its critical tumor-suppressive function.